白细胞介素-32在大鼠肾脏缺血再灌注损伤中的作用及其机制

目的:探讨白细胞介素-32(Interleukin,IL-32)在大鼠肾缺血再灌注(ischemia-reperfusion injury,IRI)损伤中的作用及其机制。方法:80只雄性SD大鼠随机分为4组:假手术组(S组,n=20)、缺血再灌注组(I/R组,n=20)、缺血前IgG抗体预处理组(IgG+I/R组,n=20)和缺血前IL-32抗体预处理组(Anti-IL-32+I/R组,n=20)。采用夹闭双侧肾蒂30min后恢复血供的方法制备肾脏缺血再灌注损伤模型,再灌注3h、6h、12h、24h分别处死大鼠收集血样和肾脏样本,自动生化分析仪测定血清中肌酐(Cr)、尿素氮(BUN)浓度,酶联免疫吸附试验(ELISA)检测大鼠血清IL-32、TNF-α、IL-1β的表达,化学比色法检测肾组织髓过氧化物酶(MPO)的活性。结果:与S组比较:1、血清Cr、BUN浓度,I/R、IgG+I/R组均显著升高(P0.05),Anti-IL-32+I/R组无显著性差异(P0.05);2、血清IL-32、TNF-α、IL-1β水平,I/R、IgG+I/R组均显著升高(P0.05),Anti-IL-32+I/R组无显著性差异(P0.05);3、肾组织MPO活性,I/R、IgG+I/R组显著增强(P0.05),Anti-IL-32+I/R组无显著性差异(P0.05)。结论:IL-32在肾脏缺血再灌注损伤后的大鼠血清中高表达,阻断IL-32能减少炎症因子释放、抑制中性粒细胞聚集,减轻肾功能损害。     

乳化异氟醚后处理对兔在体心脏缺血/再灌注损伤的保护作用

目的观察乳化异氟醚后处理对兔在体心肌缺血/再灌注损伤的影响并探讨线粒体ATP敏感性钾通道(KATP)在其中的作用。方法76只♂新西兰白兔,建立心脏30min缺血/180min再灌注损伤模型,随机分为10组:缺血对照组(CON,n=8)、缺血后处理组(IPO,n=8)、1.0MAC吸入异氟醚后处理组(ISO,n=8)、1.0MAC乳化异氟醚后处理组(EPO,n=8)、脂肪乳组(INT,n=7)、Glibenclamide组(GLI,非选择性KATP通道阻滞剂,0.3mg.kg-1,n=7)、5-hydroxy-decanoate组(5-HD,线粒体KATP通道阻滞剂,5mg.kg-1,n=8)、0.3mg.kg-1GLI+1.0MAC EPO组(GLI+EPO,n=8)、5mg.kg-15-HD+1.0MAC EPO组(5-HD+EPO,n=7)、Dimethylsulfoxide组(DMSO,GLI的溶剂,n=7)。观察血流动力学指标,缺血区(AAR)重、梗死区(IS)重,心肌梗死面积(以IS/AAR表示),再灌注180min测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)活性。结果与CON组比较,IPO组、ISO组和EPO组IS/AAR及血清CK、LDH活性均明显降低(P<0.05);与EPO组比较,EPO+GLI组、EPO+5-HD组IS/AAR明显增加,血清CK、LDH活性明显升高(P<0.05)。结论乳化异氟醚可模拟缺血后处理减轻兔在体心肌缺血/再灌注损伤,这种心肌保护作用可能与线粒体KATP通道的激活有关。     

卡托普利后处理对再灌注损伤鼠肺血管紧张

目的探讨卡托普利后处理对大鼠肺缺血—再灌注时肺血管内皮血管紧张素转换酶(ACE)mRNA表达的影响,分析其可能的作用机制。方法实验大鼠24只,随机分为假手术组(Sham组,n=8只)、缺血—再灌注组(I/R组,n=8只)和卡托普利后处理组(CAP组,n=8只)。I/R组阻断左肺门1 h后,恢复通气再灌注1 h。Sham组开胸游离左肺门,通气及灌注2 h。CAP组于再灌注前20 min腹腔注射卡托普利(10 mg.kg-1)行药物后处理,恢复通气再灌注1 h。留取静脉血及左侧肺组织,分别测定肺组织中髓过氧化物酶(MPO)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量、ACE mRNA的表达量及静脉血中ET-1的含量,测肺湿/干重比(W/D)及光镜下观察肺组织病理变化。结果 CAP组肺组织MPO、MDA的含量及ACE mRNA的表达量、血清ET-1含量及肺W/D明显低于I/R组(P0.05);CAP组肺组织中SOD含量明显高于I/R组(P0.05);CAP组肺组织形态学损伤较I/R组明显减轻。结论卡托普利后处理可以明显减轻鼠肺缺血再灌注损伤,其机制可能与其抑制缺血再灌注损伤鼠肺组织中ACE mRNA的表达有关。     

盐酸替罗非班对兔心肌缺血再灌注损伤的影响

目的:探讨盐酸替罗非班(tirofiban hydrochloride,TH)在兔心肌缺血再灌注(ischemia reperfusion,IR)损伤中的作用及其机制。方法:30只雄性新西兰大白兔随机分为3组:假手术组(S组)、心肌I/R模型组(I/R组)和心肌I/R+盐酸替罗非班治疗组(I/R+TH组),每组10只。采用结扎冠状动脉前降支1h后恢复血供的方法制备心肌I/R损伤模型,再灌注0、1、2、4h分别收集血样,酶联免疫吸附法(ELISA)测定血清中肌钙蛋白T(TnT)及炎症因子(IL-32、TNF-α及IL-1β)的水平,再灌注后4h处死动物,化学比色法检测心脏组织中髓过氧化物酶(MPO)的活性。结果:TnT水平,再灌注4h,I/R、I/R+TH组均较S组显著升高(P0.05);炎症因子水平,缺血再灌注后I/R、I/R+TH组均较S组显著升高(P0.05),I/R+TH组在再灌注1、2h有明显改善,组间两两比较,差异有统计学意义(P0.05);MPO活性,与S组比较,I/R组显著增强(P0.05),I/R+TH组差异无统计学意义(P0.05)。结论:盐酸替罗非班对兔心肌I/R损伤具有保护作用,其机制与减少炎症因子释放、降低MPO活性,抑制中性粒细胞聚集有关。     

参麦注射液对抗大鼠心肌缺血再灌注性心律失常作用

目的:探讨参麦注射液对抗大鼠心肌缺血再灌注性心律失常的影响及其作用机制.方法:结扎/松解Wistar大鼠左冠状动脉前降支,建立假手术组(Sham)、缺血组(MI)、再灌注组(MI/R)、参麦组(SM)动物模型.动态Ⅱ导联心电图监测各组心律失常发生率及持续时间,再灌注15 min和60 min S-T段改变;免疫组化技术和图像分析技术检测心肌细胞内HSP70表达;硫代巴比妥酸(TBA)法和黄嘌呤氧化酶法分别测心肌组织丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力;优化紫外分光光度法测血清肌酸激酶(CK)活性.结果:(1)SM组心律失常发生率及持续时间均明显低于其他各组,S-T段降低(P＜0.05).(2)SM组心肌组织HSP70表达量、SOD活力高于MI/R组(P＜0.05),MDA含量及血清CK活性低于MI/R组(P＜0.05).结论:参麦注射液有效地对抗再灌注损伤所致的心律失常的发生率及持续时间,其作用机制可能与增加再灌注心肌组织HSP70含量、SOD活性,减少膜脂质过氧化,稳定膜结构有关.     

异氟醚预处理延迟相对兔缺血再灌注心肌Bcl-2蛋白表达及IL-10水平的影响

目的:探讨异氟醚预处理延迟相对缺血再灌注心肌的保护作用及其机制。方法:30只健康新西兰雄性大白兔随机分成3组:假手术组(C组)、缺血再灌注组(I/R组)、2.0%异氟醚预处理延迟相组(S组),每组10只。C组仅开胸160min,I/R组行左冠脉阻断40min,再灌注120min,S组吸入2.0%异氟醚2小时,24小时后处理同I/R组。各组分别于左冠脉阻断前20min(T1)、左冠脉阻断20min(T2)、左冠脉阻断40min(T3)、再灌注1小时h(T4)、再灌注2小时(T5)5个时点抽血测血清IL-10水平。再灌注结束后免疫印迹法测心肌Bcl-2表达水平,用伊文思蓝和TTC染色测心肌梗死面积。结果:与I/R组比,S组IL-10水平增高(P<0.05),Bcl-2表达增高(P<0.05),心肌梗死面积减少(P<0.05)。结论:异氟醚预处理延迟相通过上调心肌Bcl-2表达和IL-10生成来减轻缺血再灌注损伤发挥保护作用。     

参麦注射液对再灌注性大鼠心肌细胞保护的研究

目的:探讨参麦注射液对再灌注性大鼠心肌细胞保护的作用机制.方法:结扎冠状动脉前降支复制大鼠心肌缺血再灌注损伤模型,测定心肌组织丙二醛(MDA)含量及结构型、诱导型一氧化氮合酶(cNOS,iNOS)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、血清肌酸激酶(CK)的活性.结果:参麦注射液组心肌组织cNOS、SOD、GSH-Px活性高于缺血再灌注组(P＜0.01),MDA含量、iNOS及血清CK活性低于MI/R组(P＜0.01).结论:参麦注射液保护心肌再灌注性损伤的作用与其抑制iNOS活性、激活cNOS、提高心肌抗氧化能力、清除氧自由基、减轻细胞膜脂质过氧化状态相关.     

冠心宁注射液对大鼠心肌缺血再灌注损伤的保护作用

目的:观察冠心宁注射液对大鼠心肌缺血再灌注损伤的保护作用,探讨冠心宁抗心肌缺血再灌注损伤的保护机理.方法:雄性SD大鼠30只随机分成假手术组(C组)、缺血再灌注组(I/R组)、冠心宁治疗组(G组),建立大鼠在体心肌缺血再灌注模型:C组丝线穿过冠状动脉前降支但不结扎,I/R、G组通过结扎心脏左冠状动脉前降支40 min,再灌注60 min制作缺血再灌注损伤动物模型.缺血前30 min,G组经腹腔注射冠心宁注射液10.0 ml·kg-1,余两组注射等量0.9%氯化钠注射液.测定再灌注60 min后心肌超氧化物岐化酶(SOD)活性及丙二醛(MDA)含量,同时取每组大鼠心肌检测梗死面积,电镜下观察缺血区心肌超微结构变化.结果:与I/R组相比,G组再灌注后60 min心肌MDA含量降低(P<0.01),SOD活性增高(P<0.01),梗死面积较小(P<0.01),心肌超微结构受损较轻.结论:冠心宁注射液对心肌缺血再灌注损伤有明显的保护作用,其机制与其增强心肌抗氧化作用有关.     

丹参素钠通过抑制炎症反应对心肌缺血-再灌注损伤的保护作用

目的探讨丹参素钠通过抑制炎症反应对大鼠心肌缺血-再灌注(myocardial ischemia-reperfusion,MI/R)损伤的保护作用。方法采用结扎冠状动脉复制大鼠MI/R损伤模型,将动物随机分为假手术组,模型组,丹参素钠低、中、高剂量组。除模型组于再灌注时给予生理盐水外,丹参素钠低、中、高剂量组于再灌注即刻给予丹参素钠(15、30、60 mg kg-1)。实验终末,测定心肌梗死面积,检测血清中肌酸激酶同工酶(CK-MB)、肌钙蛋白(cTnI)、肿瘤坏死因子(TNF-α)、白细胞介素1(IL-1)和白细胞介素6(IL-6)水平,采用苏木精-伊红染色法(HE)观察心肌组织的病理性改变。结果与模型组相比,丹参素钠中、高剂量组大鼠心肌梗死面积显著减少(P<0.05),血清中CK-MB、cTnI的浓度显著下降(P<0.05),并且丹参素钠高剂量组TNF-α、IL-1、IL-6均显著小于模型组(P<0.05),所有给药组心肌组织的病理损伤也小于模型组。结论丹参素钠对大鼠MI/R损伤有保护作用,其机制与抑制MI/R损伤时的炎症反应相关。     

大鼠急性肾缺血再灌注时心肌细胞氧化损伤及瑞芬太尼的干预作用

目的观察大鼠急性肾缺血再灌注时心肌细胞氧化损伤以及瑞芬太尼预处理对氧化损伤的干预作用。方法建立大鼠肾缺血再灌注损伤模型。将54只Wistar大鼠随机分为假手术组(Sham组)、缺血再灌注组(I/R组)、瑞芬太尼预处理组(R组)。Sham组只结扎单侧肾脏,另一侧只穿线不结扎;I/R组结扎右侧肾脏,动脉夹夹闭左侧肾蒂45min后开放,于再灌注30min、1、2、3h处死大鼠;R组为缺血前以1μg·kg-1·min-1微泵输注瑞芬太尼30min进行预处理,余同I/R组。分别检测各组大鼠心肌组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及谷胱甘肽过氧物酶(GSH-Px)活力变化。结果I/R组、R组与Sham组相比,心肌组织MDA含量升高,SOD、GSH-Px活力降低,且在1、2、3h时间点,差异均有统计学意义(P<0.05)。R组与I/R组比较,心肌组织MDA含量降低,SOD、GSH-Px的表达增高,且差异有统计学意义(P<0.05)。结论大鼠急性肾缺血再灌注可造成心肌细胞氧化损伤,而瑞芬太尼预处理可起到一定的保护作用。     

Cardioprotective effects of the vasodilator/beta-adrenoceptor blocker, carvedilol, in two models of myocardial infarction in the rat.

The purpose of this study was to evaluate the cardioprotective effects of carvedilol, a beta-adrenergic blocker and vasodilator, in two models of ischemic myocardial damage in the rat. Following coronary artery occlusion for 0.5 h and reperfusion for 24 h (MI/R group), left ventricular (LV) injury was determined by planimetric analysis of triphenyltetrazolium chloride-stained tissue, and polymorphonuclear leukocyte infiltration was assessed by measuring myeloperoxidase (MPO) activity. In the vehicle-treated MI/R group, infarct size was 14.2 +/- 1.3% of the LV (n = 16), and MPO activity was increased to 2.8 +/- 0.7 from 0.14 +/- 0.03 U/g tissue in the vehicle-treated sham-occluded group (p less than 0.01). Carvedilol (1 mg/kg i.v., 15 min prior to coronary artery occlusion and at 3.5 h following reperfusion) reduced myocardial infarct size to 7.5 +/- 1.2% of the LV (n = 14; p less than 0.01) and attenuated the increase in MPO activity to 1.4 +/- 0.4 U/g tissue (p less than 0.05). A lower dose of carvedilol (i.e. 0.3 mg/kg i.v.) did not limit myocardial infarct size or the increase in MPO activity. In a model of permanent coronary artery occlusion, 24-hour survival was reduced from 85% in sham-occluded animals (n = 38) to 44% in the vehicle-treated MI group (n = 84; p less than 0.01). In comparison to the vehicle-treated MI group, carvedilol (0.3 mg/kg i.v., 15 min prior to coronary artery occlusion and 1 mg/kg 4 h after occlusion) improved survival by 55% (n = 64; p less than 0.05, compared to the vehicle-treated MI group), whereas the same dose of propranolol (n = 42) had no significant effect on survival. These results indicate that carvedilol reduces myocardial ischemia/reperfusion injury, and significantly improves survival in a permanent coronary artery occlusion model of myocardial infarction.     

Daltroban, a thromboxane receptor antagonist, protects the myocardium against reperfusion injury following myocardial ischemia without protecting the coronary endothelium

The effects of daltroban, a specific thromboxane receptor antagonist, were investigated in a model of myocardial ischemia consisting of 1.5 h of coronary artery occlusion followed by reperfusion for 4.5 h in anesthetized cats. Daltroban (1 mg/kg) was infused as a bolus 10 min prior to reperfusion of the left anterior descending (LAD) coronary artery. Daltroban infusion resulted in a significantly lower necrotic area expressed as a percentage of the myocardial area-at-risk compared to the MI + vehicle group. However, daltroban failed to retard increases in myeloperoxidase activity in the ischemic myocardium, indicating no reduction in neutrophil accumulation. Moreover, left anterior descending coronary artery ring preparations isolated from daltroban treated MI cats exhibited endothelial dysfunction following ischemia reperfusion. Thus, daltroban significantly protected the myocardium from reperfusion injury without protecting the coronary endothelium or retarding neutrophil accumulation.     

Pterostilbene protects against myocardial ischemia/reperfusion injury via suppressing oxidative/nitrative stress and inflammatory response

Recent studies have shown that pterostilbene (Pte) confers protection against myocardial ischemia/reperfusion injury. The oxidative/nitrative stress and inflammation induce injury after myocardial ischemia/reperfusion. The present study was designed to evaluate whether treatment with Pte attenuates oxidative/nitrative stress and inflammation in myocardial ischemia/reperfusion (MI/R). Rats were subjected to 30 min of myocardial ischemia and 3 h of reperfusion, and the rats were administered with vehicle or Pte. The results showed that Pte (10 mg/kg) dramatically improved cardiac function and reduced myocardial infarction and myocardial apoptosis following MI/R. As an indicator of oxidative/nitrative stress, myocardial ONOO⁻ content was markedly reduced after Pte treatment. And, Pte led to a dramatic decrease in superoxide generation and malondialdehyde (MDA) content and a dramatic increase in superoxide dismutase (SOD) activity. In addition, Pte treatment significantly reduced p38 MAPK activation and the expression of iNOS and gp91^phox and increased phosphorylated eNOS expression. Pte treatment dramatically decreased myocardial TNF-α, and IL-1β levels and myeloperoxidase (MPO) activity. Furthermore, ONOO⁻ suppression by either Pte or uric acid (UA), an ONOO⁻ scavenger, reduced myocardial injury. In conclusion, Pte exerts a protective effect against MI/R injury by suppressing oxidative/nitrative stress. These results provide evidence that Pte might be a therapeutic approach for the treatment of MI/R injury.     

心肌缺血再灌注中TNF动态变化及药物干预

目的探讨肿瘤坏死因子(TNF)、髓过氧化物酶(MPO)在心肌缺血再灌注(MI/R)中的动态变化的临床意义及卡托普利的干预作用。方法将实验兔54只分为MI/R组、卡托普利治疗组及假手术对照组,分别测缺血前、缺血0.5h,再灌注0.5、1.5、6h5个时相点外周血TNF,以及后4个时相点心肌组织TNF、MPO含量,对照组心肌指标只检测最后一个时相点。结果再灌注0.5h外周血TNF即开始升高(P<0.05),再灌注6h更高(P<0.01),心肌组织TNF、MPO含量则于再灌注1.5h升高并持续至再灌注6h,卡托普利干预后上述指标均有明显改善。结论TNF参与再灌注损伤,是再灌注后导致内皮功能紊乱的重要因素之一。卡托普利通过保护内皮,减少致伤因素而减轻再灌注损伤。     

Effect of propranolol on ischemic myocardial damage and left ventricular hypertrophy following permanent coronary artery occlusion or occlusion followed by reperfusion

This study was designed to assess the effect of propranolol for limiting myocardial damage and hypertrophy in rats with permanent coronary artery occlusion or occlusion followed by reperfusion. Rats were subjected to occlusion of the left main coronary artery for 48 h (MI) or 0.5 h of occlusion followed by reperfusion for 47.5 h (MI/R). Myocardial injury was determined by measuring the depletion of creatine phosphokinase (CK) levels from the left ventricular free wall. In comparison to sham-occluded animals, myocardial CK levels were significantly decreased by 40% in MI + vehicle animals and 30% in MI/R + vehicle animals. Propranolol (0.3 mg/kg 1 min before occlusion followed by 1 mg/kg at 4 and 24 h after occlusion) significantly reduced the loss of myocardial CK-specific activity in MI animals, but failed to prevent the loss of CK-specific activity in animals subjected to coronary artery reperfusion. Left ventricular hypertrophy developed to a similar extent in both vehicle-treated MI and MI/R groups. Propranolol had no effect on the myocardial hypertrophy in MI or MI/R animals. Likewise, in MI/R animals no diminution of polymorphonuclear leukocyte infiltration was seen with propranolol. These data indicate that propranolol had a significant cardioprotective effect in rats with permanent coronary artery occlusion but failed to salvage ischemic tissue, reduce myocardial hypertrophy or mitigate neutrophil infiltration in animals with early reperfusion of the ischemic myocardium. These results suggest that propranolol may afford a significant protection of the ischemic myocardium, but the combination of reperfusion and propranolol may not result in any greater reduction in infarct size than reperfusion alone.     

Alpha-lipoic acid protects against myocardial ischemia/reperfusion injury via multiple target effects

Myocardial ischemia/reperfusion (MI/R) is a major cause for the events of cardiovascular disease. Oxidative stress plays a critical role in the development of ischemia/reperfusion (IR) injury. As a potent antioxidant, alpha-lipoic acid (LA) has been shown to provide a benefit for the inhibition of IR injury and inhibit reactive oxygen species (ROS) generation during MI/R in rats. However, the mechanism on the protective effect of LA is still to be clarified. The present study was aimed to investigate the protective effect of LA against MI/R injury and its mechanisms. We found that 2 h of myocardial ischemia followed by different time periods of reperfusion resulted in significant increase of creatine kinase (CK) activity. MI/R also significantly promoted oxidative stress and decreased the activities of antioxidant enzymes. In addition, apoptosis and inflammatory response were activated and aggravated in a time-dependent manner by MI/R. All these alterations induced by MI/R were attenuated by the administration of LA 30 min before reperfusion. These results suggested that LA played a protective effect against MI/R injury via antioxidant, anti-apoptotic and anti-inflammatory effects. These findings may significantly better the understanding of the pharmacological actions of LA and advance therapeutic approaches to MI/R injury and cardiovascular diseases.     

Myocardial salvage by trolox and ascorbic acid,but not ascorbic acid alone,in anesthetized dogs and rabbits

The myocardial salvaging properties of Trolox (Trix; a water- and lipid-soluble vitamin E analog with antioxidant properties) and ascorbic acid (Asc; a water-soluble antioxidant) were evaluated in anesthetized male dogs and rabbits. Myocardial infarction (MI) was induced by occlusion and reperfusion of the left anterior descending coronary artery: a 2-hr occlusion and 4-hr reperfusion in dogs, and a 15-min occlusion and 3-hr reperfusion in rabbits. This occlusion/reperfusion protocol induced %MI (MI normalized to area at risk) of approximately 20% beyond that induced by occlusion alone in both species. Trlx, Asc (100 and 150 mg/kg/injection, respectively, by injection; or 100 and 150 mg/kg/min, respectively, by continuous infusion), or vehicle (Veh) were administered into the ascending aorta in dogs and into the left atrium in rabbits. In severely ischemic dogs (myocardial collateral blood flow < 0.1 ml/min/g), a single injection of Trlx plus Asc, but not Asc alone, at the onset of reperfusion reduced %MI (Trlx + Asc = 24.3 ± 5.4%, n = 7; Asc = 50.1 ± 9.6%, n = 4; Veh = 45.0 ± 5.0%, n = 5). In rabbits, %MI was reduced (or tended to be reduced) by either 3 hourly injections (Trlx + Asc = 33.3 ± 4.0%, n = 19; Asc = 48.3 ± 6.3%, n = 11; Veh = 43.7 ± 3.3%, n = 8) or an injection followed by continuous infusion (Trlx + Asc = 36.0 ± 4.0%, n = 9; Veh = 49.0 ± 3.0%, n = 8), beginning at the onset of reperfusion. %MI in rabbits was not affected by either hourly injections beginning from 1 hr after, or a single injection at 1–3 × the dosages (i.e., 100–300 and 150–450 mg/kg for Trlx and Asc, respectively), during onset of reperfusion. Hemodynamic variables (arterial pressure, heartrate, rate-pressure-product and left ventricular contractility) were similar among all treat- ment groups in both species. In conclusion, Trlx/Asc combination, but not Asc alone, re- duces %MI in dogs and rabbits. The salvaging effects of Trlx/Asc are unrelated to any changes in hemodynamics. These results are consistent with the hypothesis that lipid peroxidation is involved in myocardial reperfusion injury. © 1992 Wiley-Liss, Inc.     

具栖冬青苷对大鼠急性心肌缺血/再灌注损伤的保护作用研究

目的研究具栖冬青苷(pedunculoside,PE)对大鼠急性心肌缺血/再灌注损伤(MIRI)的保护作用。方法采用结扎大鼠心脏冠状动脉左前降支(LAD)30 min,再灌注24 h的方法制备急性心肌缺血/再灌注损伤模型。大鼠随机分为7组(n=10),即假手术组(Sham)、急性心肌缺血/再灌注损伤模型组(M)、卡托普利组(Capt,阳性药)、美托洛尔组(MT,阳性药)、PE低、中、高剂量组(2.5 mg·kg-1、5 mg·kg-1和10 mg·kg-1)。术前连续给药3 d,每日1次。观察PE对MIRI大鼠心肌缺血/再灌注损伤的影响。结果MIRI模型组大鼠在结扎LAD 30 min,再灌注24 h后,心肌梗死面积显著增加,心脏收缩、舒张功能降低,表现为LVSP、+d P/d t max降低,LVEDP、-d P/d t max升高。同时,血清SOD含量降低,MDA,CTnI含量升高。与模型组比较,PE能明显改善上述病理改变。结论具栖冬青苷对大鼠急性心肌缺血/再灌注损伤有明显的保护作用。     

阿魏酸钠保护大鼠心肌缺血再灌注损伤的作用机制研究

目的 探讨阿魏酸钠(SF)对心肌缺血再灌注(MI/R)损伤大鼠的保护作用及其机制.方法 40只SD大鼠随机分为假手术组、模型组、SF高剂量组(40 mg/kg)、SF低剂量组(20 mg/kg),每组10只.采用结扎左冠状动脉前降支30 min再灌注2 h的方法 复制MI/R损伤大鼠模型,造模成功后取心脏测定心肌梗死面积、心肌组织细胞间黏附分子-1(ICAM-1)和核因子-κB(NF-κB)表达情况及髓过氧化物酶(MPO)的活力.结果 SF高、低剂量组心肌梗死面积小于模型组(P<0.05,P<0.01).模型组心肌MPO活力和ICAM-1、NF-κB阳性表达率高于假手术组,SF高、低剂量组均低于模型组(P<0.05,P<0.01).结论 SF对心肌MI/R损伤的保护作用是通过抑制中性粒细胞浸润,下调NF-κB和ICAM-1的表达,抑制炎性反应等途径实现的.     

雌激素对兔脊髓缺血再灌注损伤的保护作用

目的：探讨雌激素对兔脊髓缺血再灌注损伤的神经保护效应。方法成年新西兰大白兔肾下腹主动脉钳夹20min恢复再灌注。实验分组如下：Control组（n=8）仅行肾下腹主动脉钳夹20min恢复再灌注;Sham组（n=8）行对照组操作除外肾下腹主动脉钳夹;雌激素处理组（n=8）分别在再灌注开始即刻经兔耳缘静脉给予雌激素200,400,800μg/kg。再灌注后48h进行下肢神经功能评分（Tarlov法）后处死受试动物,取脊髓行组织HE染色切片病理分析。结果Tarlov评分发现雌激素处理组神经功能评分明显高于control组（P＜0.05）。组织病理分析可见脊髓前角运动神经元凋亡,坏死较明显。雌激素处理组脊髓前角运动神经元计数明显多于Control组（P＜0.01）。结论兔脊髓缺血后静脉给予雌激素可明显改善下肢神经功能,增加脊髓前角正常运动神经元数量,减轻缺血再灌注损伤。